What Is Parvovirus B19?

Human parvovirus B19 was unintentionally discovered by British scientist Cossart and colleagues during the screening of asymptomatic hepatitis B patients in 1977, and was classified into the parvoviridae family based on biochemical and molecular biological characteristics.

Human parvovirus B19

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Human parvovirus B19 was unintentionally discovered by British scientist Cossart and colleagues during the screening of asymptomatic hepatitis B patients in 1977, and was classified into the parvoviridae family based on biochemical and molecular biological characteristics.

Chinese scientific name

Human parvovirus B19

nickname

Human Parvovirus B19 (HPVB19)

boundary

Virus world

Branch

Parvoviridae

Yaco

Parvoviridae

Genus

Red Vision Virus

Species

Human parvovirus B19

Human parvovirus B19

Human Parvovirus B19

Species

Parvoviridae> Parvoviridae> Red Vision Virus> Human Parvovirus B19

Since it was found in sample No. 19 of group B, it was named B19 virus. Initially, B19 was thought to be a virus that was widespread and non-pathogenic in the population, but it was later discovered that B19 infection caused infectious erythema, aplastic anemia in patients with chronic hemolytic anemia, chronic anemia in immunosuppressed patients, abortion during pregnancy, Pathogen of stillbirth.

Human parvovirus B19 is common

Human parvovirus B19 has a special tropism for human red blood cells. This virus can grow in fresh human bone marrow cells, peripheral blood cells, fetal liver cells, red leukemia cells, and umbilical cord blood cells, but its reproduction depends on any culture system. In the presence of red blood cells and specific erythropoietin, cell sensitivity increases with red blood cell differentiation. The above system can be used to study the characteristics of the virus, but it cannot be used for specimen isolation. The B19 virus has a direct cytotoxic effect on host cells and can cause changes in the ultrastructure of pre-erythrocytes, including characteristic chromatin migration, pseudopod formation, and vacuoles. The shell protein particles are present in the nucleus of the apoptotic cell. in. Recently, the receptor of B19 virus was identified as erythrocyte glycosides or erythrocyte P antigen. They have a high affinity for the virus. P antigen is also expressed in megakaryocytes, endothelial cells, and fetal liver cells. Some individuals lack P antigen, and therefore have no response to B19. Virus infection is not sensitive.

Human parvovirus B19 infection is also one of the important causes of congenital heart disease. B19 virus has an affinity for fetal cardiomyocytes, and fetal B19 virus infection can cause myocardial swelling and degeneration. B19 virus detection and in situ localization of congenital heart disease biopsy myocardial tissue and autopsy myocardial tissue revealed that B19 virus has a higher positive detection rate in myocardial cells of congenital heart disease, and viral DNA is localized in the nucleus of myocardial cells, and myocardial cells themselves Inflammatory response, which indicates that B19 virus may be one of the causes of congenital heart disease.

Young children are often infected with the B19 virus. After being infected with the virus, some children's cheeks are pink and tender and look like apples. This is medically called infectious erythema. The B19 virus only infects humans and a few monkeys, and is a human-specific virus. Infectious erythema occurs in children aged 2-10 years, and there is no specific epidemic season, but it is more common in late winter and early spring. The general incubation period is several days to two weeks. It is contagious and can be transmitted through air and contact.

At the beginning of the onset, there may be precursor symptoms such as slight fever, rhinitis, and headache. One to two days later, a facial rash began to appear, often with itching. One to four days after the erythema on the cheek disappears, erythema will begin to appear on the proximal end of the trunk and limbs; then the center of the erythema on the body fades, making the erythema look like lace or mesh, and then fades within one to two weeks. In some cases, about one month after recovery, if the temperature changes, exercise, emotional excitement or sunlight exposure, it may still recur, but the symptoms are mild.

For generally healthy people, infectious erythema is mostly free of complications. But about 10% of children with infectious erythema develop joint disease. In addition, in some patients with chronic hemolytic anemia, severe anemia may be caused. Because infectious erythema is a self-limiting disease, the prognosis is good, and no special treatment is needed. A few symptomatic patients (such as arthritis, itchy skin, etc.) can be treated symptomatically. Although infectious erythema is contagious, it is limited to before the rash, when the rash appears, the child is no longer contagious, so no special isolation is needed.

B19 virus infection is an acute biphasic disease. By intranasal vaccination of volunteers, the virus can be detected in blood on the 5th to 6th days, peaking on the 8th to 9th days, with nonspecific acute influenza-like symptoms accompanied by viremia, and specific antibody production 10-14 days after the inoculation. With typical symptoms of EI, volunteers have systemic rash and arthritis, bone marrow suppression is consistent with viremia, and transient aplastic anemia is an early manifestation of infection.

The treatment of infectious erythema and TAC is currently limited to symptomatic treatment, and antiviral therapy is effective for persistent B19 virus infection. Commercially available immunoglobulin preparations are a good source of neutralizing antibodies. Patients with congenital immunodeficiency are given 400 mg / kg intravenous injection of immunoglobulin daily for a course of 10 days by intermittent injections until the serum level is measured. Until the virus. AIDS patients have a course of 5-10 days. Although it will recur after a few months, re-use is still effective.

B19 virus infection is distributed worldwide and can occur all year round, with peaks in winter and spring. Outbreaks of common EI in children are about every 3-4 years. Transient TAC outbreaks in hemolytic patients tend to be at the same time. About 50% of adults have B19 virus IgG antibodies, and the proportion of elderly people has increased to 90% Each year, the rate of seroconversion reaches 1.5%. Therefore, most individuals have been immunized in childhood, but the infection rate is still high during the epidemic period. 10% to 60% of susceptible school-age children can develop EI and have familial aggregation.

B19 virus can be transmitted through blood transfusion or damaged skin (tattoo). It is most common in patients who receive condensed factor therapy. Respiratory tract is currently found to be the route of B19 virus infection and detoxification, and direct close contact is the most likely mode of transmission. In addition, the transmission of B19 virus from donor to recipient during mother-to-child transmission and organ transplantation cannot be ignored.

Most patients with EI have passed the infectious period when their typical manifestations, and B19DNA cannot be detected in the respiratory tract and blood, and isolation is not required. The main clinical danger comes from patients with high titer viremia, such as patients with transient TAC or chronic simple erythrocyte aplastic disorder. These patients' serum B19 DNA is often positive and infectious. They should be isolated in the detoxification period. When you contact, you need to wear a mask. The patient's respiratory tract secretions and blood samples, excreta should be properly handled.

During the B19 virus epidemic period, immunoglobulin preparations containing neutralizing antibodies and anti-serum in human recovery period can be injected.